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[IC‐P‐196]: TAU DISTRIBUTION IN PRECLINICAL ALZHEIMER's DISEASE: FINDINGS FROM THE KNIGHT ALZHEIMER's DISEASE RESEARCH CENTER
Author(s) -
Schultz Stephanie A.,
Gordon Brian A.,
Mishra Shruti,
Su Yi,
Morris John C.,
Benzinger Tammie L.S.,
Ances Beau
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.2571
Subject(s) - dementia , pittsburgh compound b , amyloid (mycology) , medicine , clinical dementia rating , positron emission tomography , cohort , disease , alzheimer's disease , neuropathology , pathology , postmortem studies , psychology , nuclear medicine
study, n1⁄435). Results: In the BioFINDER study we found that the tau pattern involved predominantly inferior, medial, and lateral temporal cortical areas, the precuneus, and lateral parietal and occipital cortex (Figure 1). This pattern overlapped primarily with the dorsal attention, and to some extent with higher visual, limbic, and parts of the default-mode network. PET-evidenced tau pathology in the ADNI replication sample, which represented a more prodromal group of AD cases, was less pronounced but showed a highly similar spatial distribution profile, suggesting an earlier-stage snapshot of a consistently progressing regional pattern. Preliminary analyses of atrophy patterns in the BioFINDER sample suggested an overlapping pattern with tau spread but with markedly less isocortical involvement. Conclusions:Our results indicate that the regional deposition of tau aggregates in AD predominantly affects higher-order cognitive over primary sensory-motor networks, but does not appear to be specific for the default-mode or related limbic networks. Less isocortical involvement of GM atrophy may reflect a protracted process of tau-mediated neurodegeneration.